Revisiting the relationships between human well-being and ecosystems in dynamic social-ecological systems: Implications for stewardship and development

This is the final version. Available from Cambridge University Press via the DOI in this record.Non-technical summary We argue that the ways in which we as humans derive well-being from nature - for example by harvesting firewood, selling fish or enjoying natural beauty - feed back into how we behave towards the environment. This feedback is mediated by institutions (rules, regulations) and by individual capacities to act. Understanding these relationships can guide better interventions for sustainably improving well-being and alleviating poverty. However, more attention needs to be paid to how experience-related benefits from nature influence attitudes and actions towards the environment, and how these relationships can be reflected in more environmentally sustainable development projects. Technical summary In the broad literatures that address the linked challenge of maintaining ecosystem integrity while addressing poverty and inequality, there is still a need to investigate how linkages and feedbacks between ecosystem services and well-being can be taken into account to ensure environmental sustainability and improved livelihoods. We present a conceptual model towards a dynamic and reciprocal understanding of the feedbacks between human well-being and ecosystems. The conceptual model highlights three mechanisms through which people derive benefits from ecosystems (use, money and experience), and illustrates how these benefits can affect values, attitudes and actions towards ecosystems. Institutions and agency determine access to and distribution of benefits and costs, and also present barriers or enabling factors for individual or collective action. The conceptual model synthesises insights from existing but mostly separate bodies of literature on well-being and the benefits humans derive from ecosystems, and reveals gaps and areas for future research. Two case studies illustrate how recognizing the full feedback loop between how ecosystems support human well-being and how people behave towards those ecosystems, as well as intervention points within the loop, can guide better action for sustainable poverty alleviation and stewardship of the biosphere.Swedish Research CouncilSwedish Research Counci

Sprint interval and sprint continuous training increases circulating CD34+ cells and cardio-respiratory fitness in young healthy women

The improvement of vascular health in the exercising limb can be attained by sprint interval training (SIT). However, the effects on systemic vascular function and on circulating angiogenic cells (CACs) which may contribute to endothelial repair have not been investigated. Additionally, a comparison between SIT and sprint continuous training (SCT) which is less time committing has not been made

Research into the Health Benefits of Sprint Interval Training Should Focus on Protocols with Fewer and Shorter Sprints

Over the past decade, it has been convincingly shown that regularly performing repeated brief supramaximal cycle sprints (sprint interval training [SIT]) is associated with aerobic adaptations and health benefits similar to or greater than with moderate-intensity continuous training (MICT). SIT is often promoted as a time-efficient exercise strategy, but the most commonly studied SIT protocol (4–6 repeated 30-s Wingate sprints with 4 min recovery, here referred to as ‘classic’ SIT) takes up to approximately 30 min per session. Combined with high associated perceived exertion, this makes classic SIT unsuitable as an alternative/adjunct to current exercise recommendations involving MICT. However, there are no indications that the design of the classic SIT protocol has been based on considerations regarding the lowest number or shortest duration of sprints to optimise time efficiency while retaining the associated health benefits. In recent years, studies have shown that novel SIT protocols with both fewer and shorter sprints are efficacious at improving important risk factors of noncommunicable diseases in sedentary individuals, and provide health benefits that are no worse than those associated with classic SIT. These shorter/easier protocols have the potential to remove many of the common barriers to exercise in the general population. Thus, based on the evidence summarised in this current opinion paper, we propose that there is a need for a fundamental change in focus in SIT research in order to move away from further characterising the classic SIT protocol and towards establishing acceptable and effective protocols that involve minimal sprint durations and repetitions

Amiloride Analogs Cause Endothelium-Dependent Relaxation in the Canine Coronary-Artery Invitro - Possible Role of Na+/ca2+ Exchange

A number of amiloride analogues were used to test the proposal that Na/Ca exchange may play a role in the secretion of endothelium‐derived relaxing factor (EDRF). The analogues used were those substituted on either the 5‐amino group or the terminal guanidino nitrogen atom. The former block both Na /Ca and Na /H exchange whilst the latter block the Na channel and the Na /Ca exchange. Both series of compounds caused relaxation in isolated rings of dog coronary artery (EC values, 1–10 μM) presumably due to release of EDRF since removal of endothelium greatly attenuated the response. Amiloride (1–100 μM) had little effect on either endothelium‐intact or denuded arteries. The guanidino substituted analogues also appeared to block selectively the relaxation response to acetylcholine in the coronary artery, independently of their EDRF‐releasing activity. It is proposed that endothelial cells have an active Na /Ca exchange operating in the forward mode to extrude Ca. This mechanism may be important in the control of EDRF release. 1988 British Pharmacological Societ

Protease-activated receptor-2 peptides activate neurokinin-1 receptors in the mouse isolated trachea

Protective roles for protease-activated receptor-2 (PAR2) in the airways including activation of epithelial chloride (Cl-) secretion are based on the use of presumably PAR(2)-selective peptide agonists. To determine whether PAR(2) peptide-activated Cl- secretion from mouse tracheal epithelium is dependent on PAR(2), changes in ion conductance across the epithelium [short-circuit current (I-SC)] to PAR(2) peptides were measured in Ussing chambers under voltage clamp. In addition, epithelium and endothelium-dependent relaxations to these peptides were measured in two established PAR(2) bioassays, isolated ring segments of mouse trachea and rat thoracic aorta, respectively. Apical application of the PAR(2) peptide SLIGRL caused increases in I-SC, which were inhibited by three structurally different neurokinin receptor-1 (NK1R) antagonists and inhibitors of Cl- channels but not by capsaicin, the calcitonin gene-related peptide (CGRP) receptor antagonist CGRP(8-37), or the nonselective cyclooxygenase inhibitor indomethacin. Only high concentrations of trypsin caused an increase in I-SC but did not affect the responses to SLIGRL. Relaxations to SLIGRL in the trachea and aorta were unaffected by the NK1R antagonist nolpitantium (SR 140333) but were abolished by trypsin desensitization. The rank order of potency for a range of peptides in the trachea I-SC assay was 2-furoyl-LIGRL > SLCGRL > SLIGRL > SLIGRT > LSIGRL compared with 2-furoyl-LIGRL > SLIGRL > SLIGRT > SLCGRL (LSIGRL inactive) in the aorta relaxation assay. In the mouse trachea, PAR(2) peptides activate both epithelial NK1R coupled to Cl- secretion and PAR(2) coupled to prostaglandin E-2-mediated smooth muscle relaxation. Such a potential lack of specificity of these commonly used peptides needs to be considered when roles for PAR(2) in airway function in health and disease are determined